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#29031900   2017/10/16 Save this To Up

Resveratrol improved detrusor fibrosis induced by mast cells during progression of chronic prostatitis in rats.

To investigate the detrusor fibrosis and urinary dysfunction in chronic prostatitis (CP), and to investigate whether resveratrol can improve the urinary dysfunction and the underlying molecular mechanism. After rat model of CP is established by subcutaneously injecting DPT vaccine, rats are treated with resveratrol. Experiments of bladder pressure and volume test in rats are used to investigate the effect of resveratrol on urinary dysfunction in CP rats. To assess tissue fibrosis, picrosirius red staining is performed. H&E staining is performed to identify the histopathological changes. Western blot and immunohistochemical staining are used to examine the expression of c-kit, SCF,tryptase, TGF-β, Wnt and α-SMA. The results of bladder pressure and volume test show that the maximum capacity of the bladder, residual urine volume and maximum voiding are increased significantly in CP rats. CP rats show significantly increased collagen deposition in the detrusor. H&E staining show that detrusor muscle arranged in disorder with fracture from CP rats. The results of western blot and immunohistochemical staining demonstrate that the activity of c-kit/SCF and TGF-β/Wnt/β-catenin pathway, expression levels of tryptase and α-SMA in bladder detrusor of CP group are significantly increased compared with the control group. However, resveratrol treatment significantly improved these factors. mast cell activation induced by the increased expression of c-kit/SCF in CP rats, may promote detrusor fibrosis which have a close relationship with urinary dysfunction. Resveratrol can improve the dysfunction by downregulating the mast cell activation and the activity of TGF-β/Wnt/β-catenin pathway.

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Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon anti HSV (II) gB IgG1 (mo anti HCMV IE pp65 IgG1 (m anti HCMV gB IgG1 (monocl Human Epstein-Barr Virus Jurkat Cell Extract (Indu Jurkat Cell Extract (Indu Jurkat Cell Extract (Indu Jurkat Cell Extract (Indu

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#29031229   2017/10/14 Save this To Up

[(99m)Tc]duramycin for cell death imaging: Impact of kit formulation, purification and species difference.

[(99m)Tc]duramycin is a SPECT tracer for cell death imaging. We evaluated the impact of kit formulation, purification and species difference on the pharmacokinetic profile and cell death targeting properties of [(99m)Tc]duramycin in order to define the optimal conditions for (pre-)clinical use.

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#29028535   2017/10/13 Save this To Up

Baicalin and its metabolites suppresses gluconeogenesis through activation of AMPK or AKT in insulin resistant HepG-2 cells.

Scutellaria baicalensis Georgi (S. baicalensis), as a traditional Chinese herbal medicine, is an important component of several famous Chinese medicinal formulas for treating patients with diabetes mellitus. Baicalin (BG), a main bioactive component of S. baicalensis, has been reported to have antidiabetic effects. However, pharmacokinetic studies have indicated that BG has poor oral bioavailability. Therefore, it is hard to explain the pharmacological effects of BG in vivo. Interestingly, several reports show that BG is extensively metabolized in rats and humans. Therefore, we speculate that the BG metabolites might be responsible for the pharmacological effects. In this study, BG and its three metabolites (M1-M3) were examined their effects on glucose consumption in insulin resistant HepG-2 cells with a commercial glucose assay kit. Real-time PCR and western blot assay were used to confirm genes and proteins of interest, respectively. The results demonstrate that BG and its metabolites (except for M3) enhanced the glucose consumption which might be associated with inhibiting the expression of the key gluconeogenic genes, including glucose-6-phosphatase (G6Pase), phosphoenolypyruvate carboxykinase (PEPCK) and glucose transporter 2 (GLUT2). Further study found that BG and M1 could suppress hepatic gluconeogenesis via activation of the AMPK pathway, while M2 could suppress hepatic gluconeogenesis via activation of the PI3K/AKT signaling pathway. Taken together, our findings suggest that both BG and its metabolites have antihyperglycemic activities, and might be the active forms of oral doses of BG in vivo.

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#29027487   2017/10/13 Save this To Up

Effect of tauroursodeoxycholic acid on PUFA levels and inflammation in an animal and cell model of hepatic endoplasmic reticulum stress.

The aim of this study was to evaluate hepatic polyunsaturated fatty acids (PUFAs) and inflammatory response in an animal and cell model of endoplasmic reticulum (ER) stress. Rats were divided into control, tunicamycin (TM)-treated, and TM + tauroursodeoxycholic acid (TUDCA)-treated groups. Hepatic ER stress was induced by TM and the ER stress inhibitor TUDCA was injected 30 min before induction of ER stress. Liver THLE-3 cells were treated with TM and TUDCA was administered in advance to decrease cytotoxic effects. Necroinflammation was evaluated in liver sections, while cell viability was determined using a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay kit. ER stress was confirmed by immunofluorescence and Western blot analysis of C/EBP-homologous protein and 78-kDa glucose-regulated protein. Arachidonic acid (C20:4n-6), dihomo-γ-linolenic acid (C20:3n-6), eicosapentaenoic acid (C20:5n-3), and docosahexaenoic acid (C22:6n-3) in liver tissue and THLE-3 cells were determined by liquid chromatography tandem mass spectrometry (LC-MS/MS). Phospholipase A2 (PLA2), cyclooxygenase (COX), and prostaglandin E2 (PGE2) were measured in tissue and cell samples. Hepatic ER stress was accomplished by TM and was alleviated by TUDCA. TM treatment significantly decreased PUFAs in both liver and THLE-3 cells compared to controls. PLA2, COX, and PGE2 levels were significantly increased in TM-treated rats and THLE-3 cells compared to controls. TUDCA leads to a partial restoration of liver PUFA levels and decreased PLA2, COX, and PGE2. This study reports decreased PUFA levels in ER stress and supports the use of omega-3 fatty acids in liver diseases demonstrating ER stress.

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stress-associated endopla Androst-4-ene-3,17-dion-1 anti HSV (II) gB IgG1 (mo anti HCMV IE pp65 IgG1 (m anti HCMV gB IgG1 (monocl Androgen Receptor (Phosph Androgen Receptor (Phosph Rabbit Anti-Human Androge Rabbit Anti-Human Androge Androgen Receptor (Ab 650 Alkaline Phospatase (ALP) Anti beta3 AR Human, Poly

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#29026009   2017/10/13 Save this To Up

Inactivated lactobacillus promotes the protection against myocardial ischemia reperfusion injury through NF-κ B pathway.

Objectives: Although restoration of blood flow to an ischemic organ is essential to prevent irreversible cellular injury, reperfusion may augment tissue injury in excess of that produced by ischemia alone. So this experiment was designed to study the protective effects and mechanism of inactivated lactobacillus (Lac) on myocardial ischemia reperfusion injury (MIRI). Methods: MIRI rat models were established by ligation of left anterior descending coronary artery for about 30 min and then, reperfusion for 120 min and divided into control group, model group and Lac (10(6), 10(7) and 10(8)cfu/kg) groups. At the end of the test, the creatine kinase (CK) activity, lactate dehydrogenase (LDH) activity, superoxide dismutase (SOD) activity and malondialdehyde (MDA) content were assayed by corresponding kits. The heart was obtained from rats and the myocardial infarction area was determined by TTC staining and myocardial endothelial cell apoptosis rate was determined by Tunel kit. Besides, A20, IκB, NF-κB and nitric oxide synthase (NOS) were also assayed by western blot. Results: When compared with model group, Lac obviously reduces MIRI in the rat by reducing myocardial infarction area and the apoptosis rate of endothelial cells; reduce the serum CK, LDH and MDA content; increase the serum SOD activity; and suppress NF-κB signaling and NOS expression in the myocardial tissues. Conclusion: Lac pretreatment can inhibit lipid peroxidation and effectively improve MIRI caused by oxygen free radical through inhibiting NF-κB signaling.

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#28992627   2017/10/09 Save this To Up

H3 Relaxin Protects Against Myocardial Injury in Experimental Diabetic Cardiomyopathy by Inhibiting Myocardial Apoptosis, Fibrosis and Inflammation.

Apoptosis, fibrosis and NLRP3 inflammasome activation are involved in the development of diabetic cardiomyopathy (DCM). Human recombinant relaxin-3 (H3 relaxin) is a novel bioactive peptide that inhibits cardiac injury; however, whether H3 relaxin prevents cardiac injury in rats with DCM and the underlying mechanisms are unknown.

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Influenza A H3N2 Viral Ly Rabbit Anti-Influenza-A H Rabbit Anti-Influenza-A H Rabbit Anti-Influenza-A H Mouse Anti-Influenza-A HA Mouse Anti-Influenza-A He Mouse Anti-Influenza-A He Native Influenza A Virus Native Influenza A Virus Native Influenza A Virus Recombinant Influenza A V Recombinant Influenza A V

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#28988741   2017/10/09 Save this To Up

Smad7 alleviates glomerular mesangial cell proliferation via the ROS-NF-κB pathway.

The aim of this study was to demonstrate that altered gene expression of Smad7regulated NF-κB expression and ROS production on Ang II (Angiotensin II)-induced rat glomerular mesangial cell (GMC) proliferation.

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#28975970   2017/10/04 Save this To Up

Facilitation of ultrasonic microvesicles on homing and molecular mechanism of bone marrow mesenchymal stem cells in cerebral infarction patients.

Cerebral infarction, or ischemia brain stroke, is a common cerebrovascular disease. Bone marrow mesenchymal stem cells (BMSCs) are widely used to treating ischemia disease such as cardiac infarction. Ultrasonic microvesicles may help the targeting of exogenous factors via localized energy blast. Therefore, this study aims to investigate the effect of ultrasonic microvesicles on the homing of BMSCs on artery thrombosis and the associated molecular mechanisms.

1932 related Products with: Facilitation of ultrasonic microvesicles on homing and molecular mechanism of bone marrow mesenchymal stem cells in cerebral infarction patients.

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#28974974   2017/10/04 Save this To Up

Effects of salbutamol on the inflammatory parameters and angiogenesis in the rat air pouch model of inflammation.

In the present study, effects of salbutamol on the inflammatory parameters, angiogenesis, interleukin-1 beta (IL-1β) and vascular endothelial growth factor (VEGF) levels were investigated in an air pouch model of inflammation. Inflammation was induced by intrapouch administration of 1% solution of sterile carrageenan in male Wistar rats. Salbutamol (125, 250 and 500 µg/rat) and salbutamol (500 µg/rat) plus propranolol (100 μg/rat) were injected intrapouch. After 6 and 72 h, fluid inside the pouches was collected to measure volume of exudates, leukocytes number and IL-1β levels. To determine angiogenesis, the granulation tissues were dissected out and weighed 3 days after carrageenan injection, then hemoglobin concentration was assessed using a hemoglobin assay kit. In addition, amount of VEGF in the exudates was measured 72 h after induction of inflammation. Leukocyte accumulation and the volume of exudates were significantly inhibited by salbutamol administration. In addition, salbutamol decreased the production of VEGF and IL-1β. Moreover, all used doses of salbutamol significantly inhibited angiogenesis. Interestingly, effects of salbutamol on the attenuation of angiogenesis and inflammatory parameters was similar to diclofenac sodium. Co-administration of propranolol with salbutamol clearly reversed anti-inflammatory effects of salbutamol. Salbutamol can decrease acute and chronic inflammation by β2-adrenergic receptors activation. The observed IL-1β and VEGF inhibitory properties of salbutamol may be responsible for anti-inflammatory and anti-angiogenic effect of the agent.

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#28970181   2017/10/03 Save this To Up

Altered expression of genes involved in programmed cell death in primary cultured rat cerebellar granule cells acutely challenged with tetrabromobisphenol A.

In the present study, primary cultures of rat cerebellar granule cells (CGC) and the RT(2) Profiler PCR array were used to examine the effect of acutely applied brominated flame retardant tetrabromobisphenol A (TBBPA) on the expression of 84 genes related to the main modes of programmed cell death. CGC, at the 7th day of culture, were exposed to 10 or 25μM TBBPA for 30min. Then, 3, 6, and 24h later, the viability of the cells was examined by the staining with propidium iodide (PI) or using the calcein/ethidium homodimer (CA/ET) live/dead kit, and RNA was extracted for the evaluation of gene expression by RT-PCR. At 3, 6 and 24h after the treatment, the number of viable neurons decreased, according to the PI staining method, to 75%, 58% and 41%, respectively, and with the CA/ET method to 65%, 58% and 28%, respectively. In CGC analyzed 3h after the treatment with 25μM TBBPA or 6h after 10μM TBBPA, the only change in the gene expression was a reduction in the expression of Tnf, which is associated with autophagy and may activate some pro-apoptotic proteins. Six hours after 25μM TBBPA, only 2 genes were over-expressed, a pro-apoptotic Tnfrsf10b and Irgm, which is related to autophagy, and the genes that were suppressed included the anti-apoptotic gene Xiap, the necrosis-related Commd4, pro-apoptotic Abl1, 5 genes involved in autophagy (App, Atg3, Mapk8, Pten, and Snca) and 2 genes that participate in two metabolic pathways: Atp6v1g2 (pro-apoptotic and necrosis) and Tnf (pro-apoptotic, autophagy). Autophagy-related Snca and Tnf remained under-expressed 24h after treatment with 25μM TBBPA, which was accompanied by the over-expression of the pro-apoptotic Casp6, the anti-apoptotic Birc3, 2 genes related to autophagy (Htt and Irgm) and 2 genes (Fas and Tp53) that are involved in both apoptosis (pro-apoptotic) and autophagy. These results show a complex pattern of TBBPA-evoked changes in the expression of the genes involved in the programmed neuronal death, indicating no induction of programmed necrosis, an early suppression of the autophagy and anti-apoptotic genes, followed by a delayed activation of genes associated with apoptosis.

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